Early Rise of Serum hCG in Gestational Diabetes Mellitus Women With Live Birth Through Fertilization Procedure.

Gestational diabetes mellitus (GDM) is one of the most common complications of pregnancy. The characteristics of early human chorionic gonadotropin (hCG) levels and the rise pattern in patients with GDM after fertilization (IVF) are unclear. The present investigation was a retrospective cohort analysis of eligible viable pregnancies achieved through IVF in the authors' hospital between October 2015 and June 2020.

NLRP3 inflammasome activation in gestational diabetes mellitus placentas is associated with hydrogen sulfide synthetase deficiency.

The placenta may play a key role in the activation of inflammation and initiation of insulin resistance (IR) during gestational diabetes mellitus (GDM) pathogenesis. Interleukin (IL)-1β and IL-18, regulated by NLR family pyrin domain containing-3 (NLRP3) inflammasome, are important inflammatory cytokines in the initiation of maternal IR during GDM. However, the mechanism responsible for the regulatory of NLRP3 inflammasome in placenta remains unknown.

Hydrogen sulfide modulates high glucose-induced NLRP3 inflammasome activation in 3T3-L1 adipocytes.

Activation of the NACHT leucine rich repeat and pyd domains-containing 3 (NLRP3) inflammasome plays an important role in the initiation of inflammation in adipose tissue in diabetic patients. However, the mechanisms underlying this are not fully understood. Hydrogen sulfide (HS) has been shown to have anti-inflammatory properties in various cell types.

Reduced cystathionine-γ-lyase (CSE) expression is involved in high glucose induced MMP14 expression in adipocytes and adipose tissues.

In the present study, we investigate the effect of reduced cystathionine-γ-lyase (CSE) expression in high glucose induced metalloproteinases14 (MMP14) expression in adipocytes and visceral adipose tissues. Diabetic mice were prepared by injections of STZ and the expression of CSE, MMP14 in visceral adipose tissues were determined. Adipocytes were differentiated from 3T3-L1 cells and treated with high glucose (HG), HS slow-releasing compound GYY4137 or transfected with CSE siRNA.

Hydrogen Sulfide Inhibits High Glucose-Induced sFlt-1 Production via Decreasing ADAM17 Expression in 3T3-L1 Adipocytes.

Hydrogen sulfide (HS) has recently been identified as an endogenous gaseous signaling molecule. The aim of the present study was to investigate the effect of HS on high glucose- (HG-) induced ADAM17 expression and sFlt-1 production in 3T3-L1 adipocytes. Firstly, we found that HG DMEM upregulated the expression of ADAM17 and production of sFlt-1 in 3T3-L1 adipocytes.

MiR133b is involved in endogenous hydrogen sulfide suppression of sFlt-1 production in human placenta.

Increased production of soluble fms-like tyrosine kinase-1 (sFlt-1) from placenta is one of the major contributors to the development of preeclampsia. Our previous study has shown that hydrogen sulfide (HS) inhibits sFlt-1 release in placenta. In the present study, we sought to investigate whether endogenous HS affects sFlt-1 production and elucidate which HS-producing enzyme is responsible for its effect in placenta.

MiR 20a,-20b and -200c are involved in hydrogen sulfide stimulation of VEGF production in human placental trophoblasts.

Unlabelled: Hydrogen sulfide (H2S) has been implicated to angiogenesis in various tissues. We sought to investigate the role of hydrogen sulfide (H2S) in regulating production of vascular endothelial growth factor (VEGF) proteins, the key factors of angiogenesis and vasculogenesis, in placenta.

Methods: Placental tissues were obtained from pregnant women with preeclampsia and healthy pregnant women who underwent elective cesarean section.